4. To what extent are people exposed to phthalates?

SCHER has no information
on use patterns, occurrence, and human exposures to diisodecyl
(DIDP) and di-n-octyl
phthalate (DNOP). For
DEHP,
DINP,
DIBP, DNBP, and
DBP, a large number of
studies relevant to exposure and
risk assessment of
phthalates are available
including recent risk assessment reports (RAR). Therefore, the
following text only gives short summaries.

3.4.1 Exposure assessment

Detailed exposure assessment using
concentrations of
phthalates in food,
environmental media and materials including predictions by
modelling have been performed in the EU- RARs. For an additional
detailed overview on occurrence of phthalates and assessments of
human exposures, see Heudorf et al., 2007.

Conservative exposure assessments for
DEHP,
DINP,
DIBP, DNBP, and
DBP are given in the
available RARs. However, more recent studies derived human
exposures to phthalates by
biomonitoring of
metabolite excretion since this results in a more precise
estimate of average exposures and the range of exposures as
compared to exposure estimates based on
concentrations of phthalates
in environmental media and food and assumptions on uptake of
these media. The linear two-compartment model published by Kohn
et al. (2000) and David (2000) based on the creatinine adjusted
concentrations of phthalate ester metabolites in urine and the
molar fraction of the urinary excreted metabolite related to the
parent compound (Koch et al. 2004a) were used to derive
estimates of phthalate exposure in children
(Table 1).
If available, results for adults are presented for
comparison.

The most representative
biomonitoring data from
two surveys are available on
DEHP. Within the
US-National Health and Nutritition Examination Survey (NHANES)
2001-2002, information of urinary levels of phthalate
metabolites were collected from 2782 participants aged 6 years
and older (NCEH 2005). In the pilot study for the German
Environmental Survey on Children (GerES IV), urinary levels of
phthalates were determined
in random urine sample of 254 children aged 3 to 14 years
(Becker et al. 2004). In comparison to the NHANES subpopulation
of children aged 6 to 11 years, the median levels of DEHP
metabolites were slightly higher in the German samples, while
the 95th percentiles were lower. In the German sample, the
concentrations of secondary
metabolites in urine were increased in boys as compared to girls
and were significantly higher in children aged 6-7 years
compared to children in the age group 13-14 years.

While in NHANES, no differences with respect to ethnicity were
found, an association with ethnicity was observed in two other
US studies. In an investigation of 90 girls from 4 US sites
representing four racial/ethnic groups, exposure was found to
depend on ethnicity with lowest
concentrations observed for
whites and on study site with differences of factor 1.7 (Wolff
et al. 2007). These results were supported by Teitelbaum et al
(2008) who observed a very high exposure to
phthalates in 35 healthy
Hispanic and black children.

Overall, it has to be considered that the knowledge of the
toxicokinetic behaviour of
DEHP and other
phthalates in humans is
still limited and age related differences have not been
sufficiently evaluated. Despite these uncertainties, the average
exposure of children is approximately twofold higher than that
of adults. Different life style factors, eating behaviours, a
higher dietary intake compared to body weight and the ingestion
of dust from indoor surfaces may play a role. In a recent study
from Germany, both urine samples and food duplicates were
collected from 5-8 year old boys over 3 consecutive days (Heger
2007). The results indicated that diet (without beverages) was
responsible for about 50 % of the exposure derived from
biomonitoring (1.4 µg/kg
b.w. vs. 3.1 µg/kg b.w.). Thus, other important sources, which
are not yet identified, must exist. For adults, DEHP exposure is
dominated by the dietary intake (Fromme et al. 2007),
particularly from fatty foods.

Moreover, it has to be noted that using a scenario-based
indirect approach no differences between adults and children
4-10 years old could be observed but a clearly increased
exposure was calculated for children less than 4 years of age
(Wormuth et al. 2006).

Since DINP replaces
DEHP in many applications,
an increase in the exposure to DINP occurs. Between 1999 and
2004, the proportion of DEHP to total phthalate usage decreased
from 42% to 22% and the proportion of DINP and
DIDP (no data specifically
on DINP are available) increased from 35% to 58% (ECPI 2006).
Beyond this, Wittassek et al. (2007) quantified the exposure to
phthalate in 20-29 year old students from 1988 to 2003 in a
retrospective study in Germany. A continuous decrease in DEHP
exposure was observed from 1996 until 2003 with an increase in
DINP (Median: 0.2 µg/kg b.w. to0.4 µg/kg b.w.) exposure. At
present, biomonitoring
data on the metabolites of DINP or other
phthalates in children are
not available for exposure assessment and are needed.

DINP intake for children
aged 3-12 months and 13-26 months was assessed by migration data
and average mouthing times using statistical modelling (US-CPSC,
1998).Migration rates were developed from in-vitro experiments
and scaled. These data were combined into an analytical model
that used a lognormal distribution for human exposure duration,
combining estimates from the separate experiments. The results
showed a geometric mean average daily intake of 5.7 μg/child/day
(95% confidence interval of 2.5 to 12.9) for children between
ages 3 and 12 months (less then 1 μg/kg bw/day for an 8 kg
child). The distribution was very skewed, with an estimate of 5%
of children at an intake of 94.3 μg/child/day (more than 10
μg/kg bw/day for an 8 kg child) or more (95% confidence interval
50.1 to 225.6). The values for children at 13-26 months were
considerably lower with a geometric mean of less than 1
µg/child/per day.

In conclusion, the exposure data based on
biomonitoring indicate
that average exposures are well below the
TDI for
DEHP, but the DEHP body
burden may approach or even exceed the TDI in some highly
exposed groups of population. For the other
phthalates studied, the
95th percentile exposures derived are below the TDIs except for
DNBP. For DNBP, a significant part of the population may be
exposed to doses above the TDI indicating a need for further
reductions in exposures.